Leptin... something vital....is one of the dots in the connection....

[Guest guest]

Very interesting opinions here ...you know toxins store in fats....

this has to do with fats, and fat stores, and it affects cytokines and has to do with all kinds of things, and leptin relys on D and zinc......both of which I tested very deficient in........HUM.......

I wonder if it plays a role in what we deal with ? ?

Input Anyone ? ?

Leptin was my brain food for today.......it is all so confusing...

Hugs to all ~ Dede

LEPTIN, A MULTIFUNCTIONAL PROTEIN

http://www.bioscience.org/news/scientis/leptin.htm

How Does Inflammation Cause Leptin Resistance?

http://www.fatresistancediet.com/leptin-weight-loss/69-inflammation-leptin-resistance

How, exactly, does chronic inflammation cause leptin resistance?

The question and the answer lie at the very heart of the Fat Resistance Diet.

Fat biology researchers have uncovered what many believe to be the key mechanisms of leptin resistance. Dr. Flier and his colleagues at Harvard Medical School have led these efforts. They have discovered that a group of molecules involved in reducing inflammation also interfere with leptin signaling on the cell surface and inside the cell. These molecules are known as SOCS, which stands for suppressors of cytokine signaling. Two specific SOCS molecules, SOCS-1 and SOCS-3, have been shown in many animal studies, first by Flier’s group and later by other research teams, to jam the signals that leptin is supposed to deliver to brain cells and muscle cells.

Leptin, What is Leptin? About its Science, Chemistry and Structure

http://www.3dchem.com/molecules.asp?ID=154

Leptin Resistance and Reverse T3...

http://weightloss.about.com/b/2009/05/14/leptin-resistance-and-t3.htm

Insulin, Leptin, and Blood Sugar – Why Diabetic Medication Fails

http://www.naturalnews.com/025405_sugar_blood_insulin.html

VERY INTERESTING ARTICLE on how you can boost your leptin......

http://www.criticalbench.com/Leptin-Hormone.htm

LEPTI-WHA?? It’s name is Leptin (derived from the Greek word leptos, meaning “thinâ€), and it’s without a doubt the most important hormone you probably never heard of.

You see, leptin was only first discovered just over 10 years ago, and as far as weight loss is concerned, that’s extremely recent. Leptin’s function? To communicate your nutritional status to your body and brain.

Leptin levels are mediated by two things. One is your level of body fat. All else being equal, people with higher levels of body fat will have higher leptin levels than those with lower levels of body fat and vice versa. Because leptin is secreted by fat cells, it makes sense that under normal conditions there is a direct correlation between leptin levels and the amount of fat you are carrying.

Unfortunately, when you’re attempting to lose fat and begin to restrict calories, conditions are anything but “normal†and the body responds accordingly by lowering leptin levels. This is because the second mediator of blood leptin levels is your calorie intake.

Lower your calorie intake and leptin will fall, independent of body fat. So, yes, you can be overweight and still suffer from low leptin levels – just go on a diet.

So what happens when leptin levels fall and why the heck does it matter? Again, under normal conditions leptin levels are normal and the brain gets the signal loud and clear that nutrition intake is adequate. Metabolism is high and the internal environment of the body is one very conducive to fat burning.

Until you start dieting. Go on a diet and leptin levels quickly plummet (by 50% or more after only one week), sending a signal to the body that you’re semi-starved and not consuming enough calories. This puts the breaks on metabolism and creates a hormonal environment extremely conducive to fat storage.

Thyroid hormones (hormones extremely important to metabolism) respond by taking a dive and the abdominal fat-storing stress hormone cortisol skyrockets measurably. HELLO belly fat. And if that wasn’t bad enough, the appetite stimulating hormones ghrelin, neuropeptide-Y, and anandamide all hop on board to make your life even more miserable. You don’t have to remember any of those names, just remember that when leptin drops, you get seriously hungry.

Despite having a pretty good reason for its reaction, it’s pretty ironic that our bodies are primed for fat loss at every other time except when we are trying to burn fat. Wouldn’t it be great if we could maintain high leptin levels and a body primed for fat burning while dieting? It would seemingly solve all of our problems. But in order to do this, we’d have to somehow keep leptin levels high as we attempt to lose those extra pounds.

“HOW ABOUT “SUPPLEMENTING†WITH LEPTIN?â€

A couple of problems here: First, leptin is a protein based hormone, which means that it can not be taken orally (otherwise, it would simply be digested). So that rules out a leptin pill. This leaves the method of “supplemental†leptin administration to injection. And leptin injections DO indeed work, reversing the metabolic adaptations to dieting and “starvation†even while continuing to restrict calories. In 1996, Ahima et al. used leptin injections to reverse starvation-induced neuroendrocrine adaptations in mice. “Well, that’s nice and all, but I’m human.†Point taken; research with rodents doesn’t always correlate to similar findings in humans, however…

In 1999, Heymsfield et al. performed a double-blind placebo controlled study analyzing weight loss over a 24-week period in 73 obese humans. Subjects either injected daily with leptin or a placebo (i.e. bogus alternative). At the end of the 24-week period, the leptin group lost significantly more weight than the placebo and a higher percentage of fat vs. muscle. In 2002, Rosenbaum et al. administered low-dose leptin to subjects (male and female) who had dieted to a 10% decrease in body weight. During the diet period, thyroid hormone levels, 24-hr energy expenditure, and other metabolic markers substantially decreased.

The result of the leptin replacement therapy?

“All of these endocrine changes were reversed…â€Thyroid output and daily calorie burn increased back to pre-diet levels. In 2003, Fogteloo et al. showed that leptin injections “tended to reduce the decline of energy expenditure associated with energy restriction, whereas the tendency of energy intake to increase back to baseline levels in placebo-treated subjects was largely prevented in subjects treated with leptin.†Yeah, that’s a mouthful. Let me put in simple terms: not only did the leptin group experience less of a decline in metabolism, but they were also less hungry, allowing them to more easily stick to the prescribed diet.

In 2004, Welt et al. reported that leptin given to a group of women with thyroid disorder immediately raised circulating concentrations of the thyroid hormones T3 and T4. In 2005, Rosenbaum and company were at it again, again showing that energy expenditure and circulating concentrations of T3 and T4 all returned to pre-weight-loss levels with regular leptin injections. So, as theorized, keeping leptin levels high during a diet does indeed solve our dilemma by avoiding the negative metabolic (and perhaps behavioral) adaptations that calorie restriction perpetuates. The problem? Daily leptin injections are far too expensive, costing thousands and thousands of dollars per week. So, we can pretty much forget about supplemental leptin as a solution (which is probably moot anyway considering that not too many people are going to voluntarily plunge a needle into their skin daily).

A REAL Solution Now that we know that leptin injections aren’t going to save us, let’s talk about the possibility of manipulating your body’s natural leptin production. And I’ve got good news – this can indeed be done, and without involving needles or thousands of dollars. In fact, we’ll swap the injections and mounds of cash out for two things I can guarantee you’re absolutely going to love: more calories and more carbs. We know that leptin levels decrease by about 50% after only one week of dieting, but fortunately, it doesn’t take nearly that long for leptin to bump back up with a substantial increase in caloric intake. In fact, research has shown that it only takes about 12-24 hours.

So, the answer to the fat loss catch-22?

Strategic high-calorie, high-carb CHEATING.

By strategically cheating with high calorie foods (and yes, even stuff like pizza, ice cream, wings, cookies, burgers, fries, etc), you can give leptin and metabolism a major boost mid-diet which sets you up for plenty of subsequent fat loss when you resume your reduced calorie eating regimen. This means greater net fat loss week after week, and ultimately, a much more realistic, maintainable way to bring you to the body you truly want and deserve.

So what’s so special about carbs? Well, leptin, carbohydrate and insulin have been shown to have very strong ties. Calories alone don’t get the job done, as research shows that overfeeding on protein and fat has little effect on leptin. In order to get a strong leptin response from overfeeding, there needs to be plenty of carbs in the mix. In fact, the relationship is SO strong that research conducted by Boden et al. at the Temple University School of Medicine shows that leptin levels will not fall even in response to all-out fasting so long as insulin and blood sugar are maintained via IV drip.

That’s CRAZY. Because of this carbohydrate/insulin-leptin relationship, it makes sense that foods combining both carbs and fat (like pizza, burgers, cookies, ice cream, etc) work best for reversing the negative adaptations caused by dieting because of the BIG-TIME insulin response they produce. THIS is why strategic cheating with your favorite foods is so powerful. THIS is why you truly can use your favorite foods to lose fat faster than you ever could with restrictive dieting. THIS is freedom. Essentially, it’s everything “typical†dieting isn’t. With regular dieting, come week two, you’re screwed. With strategic cheating, you can literally use ANY food you want to *ensure* that you never go a single day without a body primed for fat loss.

The cheat or not to cheat? I think the choice is clear.

Do I even need to add to that? If you want to finally stop the dietary struggle and instead start getting the results you truly deserve, then you can grab ’s complete Cheat Your Way Thin at: www.ICanEatWhateverIWant.com

Weight Gain, Inflammation and Leptin Resistance at Leptin Resistance Support Forum , http://www.curezone.com/forums/fm.asp?i=346927

Hello,

I also posted this in the Lyme Disease forum, but it deals directly with Leptin resistance, which I find fascinating. Could it be that hormone signalling is at the root of our weight regulation problems? And who knew that fat tissue was so closely related to the immune system! And that fat basically acts as part of the endocrine system because it produces hormones (like leptin!)

For anyone who has, say, an inflammatory disease (Lyme), and who has, say, Leptin resistance (i.e. gained a ton of weight)...

http://www.fatresistancediet.com/chapters/fat-resistance/breakthrough-science.htm

THE FAT RESISTANCE DIETâ„¢ :

BREAKTHROUGH Science REVERSES OBESITY

LEO GALLAND, M.D.

Introduction

Americans may be the heaviest nation on the planet, but the rest of the world is following our leadership and catching up quickly. Equally dramatic—and much less known—is the scientific revolution that is changing our understanding of obesity. New research explains why excess fat by itself causes high blood pressure, diabetes, heart attacks, cancer, strokes and arthritis and allows us to re-think strategies for achieving and maintaining leanness. Obesity and its related diseases are not just about weight; they’re about the hormones produced by fat.

Doctors and scientists used to think of fat as no more than a repository of unused calories, an expanding storehouse filled up by eating more than you burn. We now know that fat is a living organ, as active and interactive as the heart or kidneys or liver, and that fat regulates itself by producing its own set of hormones. The hormones produced by fat cells are called ADIPOKINES. They can increase or decrease appetite and metabolic rate, making weight control easier or harder. The discovery of adipokines sparked a revolution in our understanding of obesity. This is the breakthrough science that is the foundation for my book The Fat Resistance Dietâ„¢ (Broadway Books, 2005)

Leptin

The revolution started in 1994 at New York’s Rockefeller University, when Dr. Friedman and his research team discovered that the fat cells of genetically obese mice failed to produce a chemical called LEPTIN. Leptin was the first adipokine, the first hormone shown to be made exclusively by fat cells. Researchers soon discovered that administration of leptin curbed the appetite and stimulated the metabolism of laboratory animals. Injecting leptin into genetically obese mice restored them to normal body weight. Leptin appeared to function as part of what scientists refer to as a negative feedback loop. When an animal is overfed and begins to gain weight, the increase in body fat leads to an increase in production of leptin, which in turn suppresses appetite and stimulates fat burning, restoring the animal to a normal lean weight. This process of internal self-correction is called "homeostasis" and it stabilizes the body’s internal state, the way a weight at the bottom stabilizes the top of a buoy bobbing in the water.

The discovery of leptin raised great hopes that a natural cure for obesity lay around the corner. Excitement gave way to disappointment. Overweight humans are not leptin deficient: the more body fat, the higher the levels of leptin in blood. For people who are chronically overweight, the problem seems to be that leptin is not doing its job of reducing appetite and stimulating fat burning. The effect of leptin is blocked. Scientists call this state LEPTIN RESISTANCE. Returning to our image of the buoy, it’s as if more and more bottom weight is needed to help the buoy stay upright, even when the water remains calm.

It’s easy to see how we created today’s weight crisis. Technology has decreased our level of physical exertion. The ready availability of high calorie, ready-to-eat foods and snacks has increased consumption. Our fat regulatory system, based on leptin, is inefficient at limiting body fat. Its primary function throughout human history has been to sense body fat for survival during famine. Many scientists believe that the main evolutionary role of leptin was not to regulate weight or appetite, but to regulate fertility. Leptin is absolutely necessary for the normal function of reproductive organs. As fat stores fall, leptin levels drop. At a given level of thinness, a woman’s ovaries stop working, solely because of leptin deficiency. This effect is seen today in thin young women with very low body fat. Leptin lets the brain know when there is enough food available to support offspring and prevents reproduction when food is scarce.

Fat also appears to regulate the processes by which the body burns fuel for energy, especially in muscle. Adiponectin is the newest fat-produced hormone in the scientific spotlight. It also plays a central role in the biology of fat. Of all the adipokines spewed out by fat cells, adiponectin seems to be the most heroic. Recent studies show that adiponectin curbs appetite and sparks the burning of fat, as does leptin. But unlike leptin, chronically overweight people don’t suffer from resistance to the hormone. They have an outright deficiency. A lack of adequate adiponectin is emerging as a significant factor in people’s inability to melt flab and stay slim.When fat stores are low, fat cells secrete adiponectin, a recently discovered adipokine. Adiponectin helps muscle cells burn fuel for energy more effectively. It acts as a kind of super-charger for maintaining strong and active muscles when stored energy reserves are low. When food is not available and fat stores drop, adiponectin rises, helping muscle cells take up more sugar from the blood and also enabling them to burn fat more thoroughly as fuel. As fat stores increase, adiponectin levels drop and the burning of fat as fuel actually becomes less complete. It’s a process that allows the body to store fat in times of plenty as a hedge.

Advice about eating less and exercising more has been a resounding failure. Diets, whether they’re low calorie, low fat or low carbohydrate, all produce initial weight loss but do a lousy job of maintaining leanness. If there’s a way that science can help us undo the damage technology has caused, then understanding and combating leptin resistance may well be the key.

Of all the theories that attempt to explain leptin resistance and suggest a way to reverse it, the one concept that best knits together everything we know about obesity and has the best chance of stopping this epidemic is the proven link between obesity, leptin and INFLAMMATION.

Inflammation is part of the body’s protective response to injury or infection. The ancient Greeks described it as an internal fire. The Romans recognized it by four attributes: redness, heat, swelling and pain. We see those attributes in medical conditions that end in "-itis": arthritis, tonsillitis, appendicitis. During the Nineteenth Century, scientists discovered that inflammation was produced by white blood cells that migrate from the blood stream and enter areas of infection or injury. Recent research has linked heart attacks and strokes to microscopic inflammation of the blood vessels. Although inflammation produces many of the symptoms associated with being sick or injured, it is a necessary part of healing.

During the Twentieth Century, scientists uncovered the chemical basis of inflammation. It became clear that inflammation could exist without redness, heat, swelling or pain and without a migration of white blood cells. Today, in the Twenty-first Century, inflammation is seen as a chemical state that can exist in all or part of your body without necessarily producing symptoms. Its presence is most accurately determined by measuring the levels of inflammatory chemicals in the inflamed tissue, or sometimes in a blood sample. Many of the chemicals associated with inflammation actually cause damage to cells. They are referred to as "mediators" of inflammation. Other chemicals are just signals that indicate inflammation is present. They are "markers" of inflammation.

The biochemical understanding of inflammation has allowed scientists to recognize that your body controls the degree of inflammation by producing anti-inflammatory substances that damp down the pro-inflammatory signals. This is the normal response of your body to all kinds of stress: a stimulus provokes a reaction and that reaction acts as a stimulus to a counter-reaction that slowly returns your body to the state that existed before the initial stimulus. The whole process is called homeostasis and the pattern involves negative feedback loops. Homeostasis requires that all components of the negative feedback loops are in working order. Chronic inflammation results from the failure of homeostasis.

How does fat itself cause inflammation? Many adipokines, even leptin itself, are mediators of inflammation. They promote and encourage the inflammatory response, wherever it might be occurring. The more fat in your body, the higher the levels of these mediators in your blood and the greater the level of inflammation in your body. Here’s a fascinating example:

We’ve known for a long time that being overweight is associated with the development of osteoarthritis, especially in the knees. Osteoarthritis is the commonest form of arthritis and is thought to result from wear and tear on the cartilage that lines joints. Osteoarthritis produces an overgrowth of bone that narrows the space in the joint and increases the likelihood of damage when the joint is moved. Doctors have thought that the reason osteoarthritis is associated with obesity is that being heavy increases the wear and tear on your knees, a simple physical explanation.=Recent research has found a chemical connection. Joint fluid in the knees of overweight people contains high levels of leptin, which is produced by fat, not by the joints themselves. Leptin in the joints causes inflammation. Leptin also triggers the production of an anti-inflammatory chemical called TGF-beta (transforming growth factor-beta). TGF-beta is part of a negative feedback loop to damp down inflammation. But one of the effects of TGF-beta is to stimulate the growth of bone, in this case producing the bony overgrowth characteristic of osteoarthritis. So the relationship between obesity and osteoarthritis is not just created by how much you weigh. It is a hormonal relationship in which the body’s normal homeostatic mechanisms go awry and produce disease.

Everyone experiences trauma to their knees during the course of their lives. Lean people, like athletes, who experience extensive, repetitive trauma, are at risk for osteoarthritis because the stimulus to inflammation and counter-inflammation is so intense. People who are overweight develop osteoarthritis because excess body fat causes an excessive inflammatory response to minor injury, which then triggers an increase in the counter-inflammatory response. The result is that both inflammatory and anti-inflammatory mediators are increased in obesity. The end result is no longer homeostasis but disease, which develops because of the unbridled activity of chemical mediators that fail in their effort to heal.

The plot gets even thicker. The inflammatory nature of fat is not only due to fat cells themselves. In addition to fat cells (adipocytes), fat also contains blood vessels and white blood cells. Fat specifically attracts a type of white blood cell called a macrophage. Macrophage literally means "large eater" and macrophages are large white blood cells that gobble up cellular debris. They are scavengers, sometimes called "garbage men of the immune system." The macrophages found in fat are major producers of inflammatory mediators, especially a substance called Tumor Necrosis Factor (TNF). TNF is well-known in medicine, because high levels of it produce much of the tissue damage and pain associated with rheumatoid arthritis and other autoimmune diseases. Fatty tissue can be laden with TNF-producing macrophages. In some animal studies, over 40% to 50% of cells found in adipose tissue were macrophages.

What are all these macrophages doing in a person’s layers of fat? Biologists don’t yet have all the answers, but one theory is that the bloated fat cells of people who are overweight actually leak or break open. Macrophages are then mobilized from the blood to move into the leaky fat tissue and clean up the mess. Once embedded in adipose tissue, macrophages begin spewing out inflammatory chemicals, especially TNF and a related mediator called Interleukin-6 (IL-6). Chemical mediators like TNF and IL-6 produced by white blood cells are called cytokines, because they increase the activity of white blood cells. (Cyto- is Greek for "cell" and kinesis means "movement or activity". Adipokines are cytokine-like chemicals produced by fat cells). Attracted by the cytokines in fatty tissue, more white blood cells move in to assist in mopping-up, releasing more cytokines and increasing the level of inflammation.

One of the more radical research findings in fat biology suggests that fat cells are actually cousins of macrophages. It appears that very young fat cells (called pre-adipocytes) can be transformed into TNF-spewing macrophages, rather than maturing into normal adipocytes. A group of French researchers discovered that pre-adipocytes become macrophages when prompted to do so by cytokines. Their finding is another example of the dynamic complexity of fat. Fat cells are intimately connected to and sometimes interchangeable with cells of the immune system. They both create and react to a wide range of hormones and mediators. Fat can be thought of as part of the immune system and part of the endocrine (hormone) system. TNF, in fact, is both a cytokine (a mediator produced by macrophages) and an adipokine (a hormone produced by fat cells). Whatever its source, TNF and its inflammatory relatives can wreak havoc with our fat-storage-and-management systems. TNF interferes with the operation of insulin, and is therefore a major contributor to insulin resistance. So, too, is another adipokine called resistin.

What we see in obesity is the swelling of fat tissue accompanied by a cacophony of cellular activity, most of it pushing the body toward a state of excess inflammation. Among the pro-inflammatory substances made by fat cells themselves are leptin, TNF, IL-6, and resistin. Add the contribution of fat-embedded macrophages and their own payload of TNF and IL-6, and biologists are beginning to view fat as a brewery of inflammatory chemicals.

The whole body is affected by this state of affairs, since inflammatory activity is not limited to fat tissue but spills over into the bloodstream. Thus, overweight people become subject to a body-wide state of chronic, low-grade inflammation, induced by fat itself.

The effect of fat on inflammation is just half of the cycle. The effects of inflammation on fat are equally intense.

When inflammation is severe, as in a life-threatening infection, it can cause tremendous weight loss. With severe inflammation, the body cannibalizes itself and both fat and muscle cells are destroyed. This is not a good way to lose weight. The breakdown of muscle is always greater than the breakdown of fat.

When inflammation is mild and chronic, producing few symptoms and only subtle changes on blood tests, inflammation has a very different effect on your metabolism. Chronic low-grade inflammation makes your brain and body resistant to the normal regulatory effects of leptin and other hormones, including insulin and cortisol. Insulin and cortisol are not adipokines. Insulin is made in the pancreas and cortisol is made in the adrenal glands. In excess, either can have a devastating effect on your attempts to lose weight. I discussed insulin in Chapter 2. High insulin levels prevent the breakdown of fat. Cortisol actually causes fat cells to grow.

One marker of inflammation that has received considerable attention over the past two years is "C-reactive protein" or CRP. Mild elevation of the level of CRP in blood is associated with obesity and with weight gain. Weight loss, on the other hand, produces a decrease in CRP. In people with a history of heart disease, mild elevation of CRP predicts an increased risk of heart attacks and strokes. In adults who develop diabetes, elevated CRP occurs before the onset of diabetes. In people with normal blood pressure, elevated CRP predicts the future development of high blood pressure. In aging adults, high CRP is associated with muscle weakness and frailty. Studies of CRP have proven the close relationship between silent, chronic inflammation and the development of the most common chronic diseases of modern society.

Inflammation and fat share a complex relationship. When inflammation is severe, as in a life-threatening infection, it can cause tremendous weight loss. With severe inflammation, both fat and muscle cells are destroyed; the breakdown of muscle is always greater than the breakdown of fat. When inflammation is mild and chronic, however, producing few symptoms and only subtle changes on blood tests, inflammation has a very different effect on your metabolism. It disrupts hormones. Acting through the complex networks of chemicals involved in homeostasis, inflammation makes your cells resistant to the normal regulatory effects of leptin and other hormones, including insulin and cortisol. I’ll say more about insulin and cortisol later. These hormones are not adipokines, but they can have a devastating effect on your attempts to lose weight. First, I want you to understand the vicious cycle that keeps you from living lean: FAT ITSELF CAUSES INFLAMMATION.

Many adipokines, even leptin itself, are chemical mediators of inflammation. Remember what I said about mediators. They are chemicals associated with inflammation that actually cause damage to cells. The more fat in your body, the higher the levels of these mediators in your blood and the greater the level of inflammation in your body. Not only does this fat-derived inflammation prevent leptin from helping you lose weight, it causes other hormonal effects that interfere with permanent weight loss. Inflammation raises the level of insulin and cortisol, two hormones that actually cause your body to make more fat.

Insulin and cortisol

Insulin is a hormone produced in your pancreas. Its best known effect is to lower blood sugar by driving sugar and other nutrients into cells, especially muscle cells. Your muscles need insulin to help them produce energy and recover from the effects of exercise. Inflammation interferes with the effect of insulin on your muscles. Just as inflammation causes leptin resistance, it is a major cause of INSULIN RESISTANCE. With insulin resistance, your muscles are not fully responsive to insulin, so they don’t efficiently burn the sugar that circulates in your blood. As a result, your blood sugar starts to rise. Your pancreas responds by releasing more insulin. When the degree of insulin resistance outpaces the ability of your pancreas to produce more insulin, diabetes occurs. Whether or not you actually develop diabetes, high levels of circulating insulin can have seriously negative effects. There are some actions of insulin that occur outside of muscle and are not impaired during insulin resistance. As insulin levels increase, these effects of insulin are felt. High insulin levels make your kidneys retain fluid, raising your blood pressure and creating that feeling of being bloated and swollen. High insulin levels prevent ce=lls from breaking down fat, making it harder to lose weight through dieting. Insulin also turns on genes that produce a number of mediators of inflammation, so with high insulin, as with high leptin, the level of inflammation in your body increases.

Your brain and your adrenal glands are attuned to the level of inflammation in your body. As inflammation increases, your brain sends a signal to your adrenal glands to produce more of a hormone called cortisol. You may be familiar with cortisone, a drug used to relieve symptoms of inflammation like itching, redness or pain. Cortisol is the natural equivalent of the drug, made in your own adrenal glands in response to stress. Cortisol naturally combats inflammation, but at a high price. Cortisol increases the amount of belly fat. It also causes fluid retention, muscle weakness, memory loss, high blood pressure, and further raises your blood sugar. The increase in blood sugar then stimulates a further increase in insulin.

Insulin is a hormone produced in your pancreas. Its best known effect is to lower blood sugar by driving sugar and other nutrients into cells, especially muscle cells. Your muscles need insulin to help them produce energy and recover from the effects of exercise. Inflammation interferes with the effect of insulin on your muscles. Just as inflammation causes leptin resistance, it is a major cause of INSULIN RESISTANCE. With insulin resistance, your muscles are not fully responsive to insulin, so they don’t efficiently burn the sugar that circulates in your blood. As a result, your blood sugar starts to rise. Your pancreas responds by releasing more insulin. When the degree of insulin resistance outpaces the ability of your pancreas to produce more insulin, diabetes occurs.

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